Lihong Ye, Ding Ye, Yu Qian, Jiayu Li, Bin Liu, Jiacheng Ying, Manli Wang, Hao Lin, Jing Guo, Xiaohui Sun, Zhixing He, Chengping Wen, Yingying Mao
{"title":"Long-term exposure to ambient air pollution and the incidence of systemic lupus erythematosus.","authors":"Lihong Ye, Ding Ye, Yu Qian, Jiayu Li, Bin Liu, Jiacheng Ying, Manli Wang, Hao Lin, Jing Guo, Xiaohui Sun, Zhixing He, Chengping Wen, Yingying Mao","doi":"10.1016/j.chemosphere.2024.143974","DOIUrl":null,"url":null,"abstract":"<p><p>The relationship between air pollution and the risk of systemic lupus erythematosus (SLE) remains inconclusive. Here, we investigated the associations between long-term exposure to ambient air pollutants and incident SLE, based on a cohort of 502,004 participants free of SLE at baseline from UK Biobank. During a median of 13.65 follow-up years, 638 patients with SLE were identified. For each increase of interquartile range in air pollutant concentrations, the hazard ratios (HRs) and 95% confidence intervals (CIs) of SLE were 1.15 (1.04-1.27) for nitrogen dioxide (NO<sub>2</sub>), 1.08 (1.00-1.17) for nitrogen oxides (NO<sub>x</sub>), 1.13 (1.03-1.24) for particulate matter with the diameters ≤2.5 μm (PM<sub>2.5</sub>), 1.06 (0.99-1.14) for particulate matter with diameter between 2.5 μm and 10 μm (PM<sub>coarse</sub>), and 1.10 (1.02-1.18) for particulate matter with diameter ≤10 μm (PM<sub>10</sub>), respectively. A non-linear relationship of PM<sub>coarse</sub> with SLE risk was detected by using restricted cubic spline models (P<sub>non-linearity</sub> = 0.009), but not for the remaining air pollutants. Furthermore, smoking and long-term exposure to PM pollutants had significant additive interaction on SLE risk, with a relative excess risk of additive interaction (RERI) of 0.07 (95% CI: 0.02-0.09) for PM<sub>2.5</sub>, and 0.05 (95% CI: 0.01-0.08) for PM<sub>10</sub>. Additive interactions were also observed for genetic risk and PM<sub>coarse</sub> (RERI: 0.04, 95% CI: 0.00-0.07) and PM<sub>10</sub> (RERI: 0.04, 95% CI: 0.02-0.06) on SLE risk. In conclusion, our findings emphasize the significance of evaluating the impacts of long-term exposure to ambient air pollutants in preventing SLE, and highlight the necessity to identify individuals who smoke and have a high genetic risk to minimize the harmful effects of air pollution on the development of SLE.</p>","PeriodicalId":93933,"journal":{"name":"Chemosphere","volume":" ","pages":"143974"},"PeriodicalIF":0.0000,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Chemosphere","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1016/j.chemosphere.2024.143974","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Long-term exposure to ambient air pollution and the incidence of systemic lupus erythematosus.
The relationship between air pollution and the risk of systemic lupus erythematosus (SLE) remains inconclusive. Here, we investigated the associations between long-term exposure to ambient air pollutants and incident SLE, based on a cohort of 502,004 participants free of SLE at baseline from UK Biobank. During a median of 13.65 follow-up years, 638 patients with SLE were identified. For each increase of interquartile range in air pollutant concentrations, the hazard ratios (HRs) and 95% confidence intervals (CIs) of SLE were 1.15 (1.04-1.27) for nitrogen dioxide (NO2), 1.08 (1.00-1.17) for nitrogen oxides (NOx), 1.13 (1.03-1.24) for particulate matter with the diameters ≤2.5 μm (PM2.5), 1.06 (0.99-1.14) for particulate matter with diameter between 2.5 μm and 10 μm (PMcoarse), and 1.10 (1.02-1.18) for particulate matter with diameter ≤10 μm (PM10), respectively. A non-linear relationship of PMcoarse with SLE risk was detected by using restricted cubic spline models (Pnon-linearity = 0.009), but not for the remaining air pollutants. Furthermore, smoking and long-term exposure to PM pollutants had significant additive interaction on SLE risk, with a relative excess risk of additive interaction (RERI) of 0.07 (95% CI: 0.02-0.09) for PM2.5, and 0.05 (95% CI: 0.01-0.08) for PM10. Additive interactions were also observed for genetic risk and PMcoarse (RERI: 0.04, 95% CI: 0.00-0.07) and PM10 (RERI: 0.04, 95% CI: 0.02-0.06) on SLE risk. In conclusion, our findings emphasize the significance of evaluating the impacts of long-term exposure to ambient air pollutants in preventing SLE, and highlight the necessity to identify individuals who smoke and have a high genetic risk to minimize the harmful effects of air pollution on the development of SLE.